NEET MDS Lessons
General Pathology
LUNG ABSCESS Lung abscess is a localised area of necrosis of lung tissue with suppuration.
It is of 2 types:
- Primary lung abscess that develops in an otherwise normal lung. The commonest cause is aspiration of infected material.
- Secondary lung abscess that develops as a complication of some other disease of the lung or from another site
ETIOPATHOGENESIS.
The microorganisms commonly isolated from the lungs in lung abscess are streptococci, staphylococci and various gram-negative organisms. These are introduced into the lungs from one of the following mechanisms:
1. Aspiration of infected foreign material.
2. Preceding bacterial infection.
3. Bronchial obstruction.
4. Septic embolism.
5. Miscellaneous (i) Infection in pulmonary infarcts, (ii) Amoebic abscesses, (iii) Trauma to the lungs. (iv) Direct extension from a suppurative focus.
Abscesses may be of variable size from a few millimeters to large cavities, 5 to 6 cm in diameter. The cavity often contains exudate. An acute lung abscess is initially surrounded by acute pneumonia and has poorly-defined ragged wall. With passage of time, the abscess becomes chronic and develops fibrous wall.
Microscopic Examination
The characteristic feature is the destruction of lung parenchyma with suppurative exudate in the lung cavity. The cavity is initially surrounded by acute inflammation in the wall but later there is replacement by exudate of lymphocytes, plasma cells and macrophages. In more chronic cases, there is considerable fibroblastic proliferation forming a fibrocollagenic wall.
DIPHTHERIA
An acute, contagious disease caused by Corynebacterium diphtheriae, characterized by the formation of a fibrinous pseudomembrane, usually on the respiratory mucosa, and by myocardial and neural tissue damage secondary to an exotoxin.
Cutaneous diphtheria (infection of the skin) can occur when any disruption of the integument is colonized by C. diphtheriae. Lacerations, abrasions, ulcers, burns, and other wounds are potential reservoirs of the organism. Skin carriage of C. diphtheriae is also a silent reservoir of infection.
Pathology
C. diphtheriae may produce exotoxins lethal to the adjacent host cells. Occasionally, the primary site is the skin or mucosa elsewhere. The exotoxin, carried by the blood, also damages cells in distant organs, creating pathologic lesions in the respiratory passages, oropharynx, myocardium, nervous system, and kidneys.
The myocardium may show fatty degeneration or fibrosis. Degenerative changes in cranial or peripheral nerves occur chiefly in the motor fibers
In severe cases, anterior horn cells and anterior and posterior nerve roots may show damage proportional to the duration of infection before antitoxin is given. The kidneys may show a reversible interstitial nephritis with extensive cellular infiltration.
The diphtheria bacillus first destroys a layer of superficial epithelium, usually in patches, and the resulting exudate coagulates to form a grayish pseudomembrane containing bacteria, fibrin, leukocytes, and necrotic epithelial cells. However, the areas of bacterial multiplication and toxin absorption are wider and deeper than indicated by the size of the membrane formed in the wake of the spreading infection.
Cholelithiasis (Biliary calculi)
- These are insoluble material found within the biliary tract and are formed of bile constituents (cholesterol, bile pigments and calcium salts).
Sites: - -Gall bladder, extra hepatic biliary tract. Rarely, intrahepatic biliary tract.
Predisposing factors:-
- Change in the composition of bile. - It is the disturbance of the ratio between cholesterol and lecithin or bile salts which may be due to Hypercholesterolaemia which may be hereditary or the 4 F (Female, Forty, Fatty, Fertile). Drugs as clofibrate and exogenous estrogen. High intake of calories (obesity).
Increased concentration of bilirubin in bile- pigment stones
Hypercalcaemia:- Calcium carbonate stones.
2- Staisis.
3- Infection.
Pathogenesis i- Nucleation or initiation of stone formation:- The nidus may be cholesterol “due to supersaturation” Bacteria, parasite
RBCs or mucous.
ii- Acceleration:- When the stone remains in the gall bladder, other constituents are added to the
nidus to form the stone.
Complications of gall stones:-
- Predispose to infection.- Chronic irritation leading to
a. Ulceration b. Squamous metaplasia & carcinoma.
Plasma Cell Pathology
A. Multiple myeloma
1. Plasma cell neoplasm that results in the proliferation of monoclonal plasma cells. These tumor cells produce nonfunctional immunoglobulins.
2. Laboratory findings include:
a. Monoclonal IgG spike.
b. Bence-Jones proteins found in urine.
3. Radiographic findings: characteristic “punched-out” radiolucencies in bones.
Fanconi’s syndrome
Characterized by the failure of the proximal renal tubules to resorb amino acids, glucose, and phosphates.
May be inherited or acquired.
Clinical manifestations include
glycosuria, hyperphosphaturia, hypophosphatemia, aminoaciduria, and systemic acidosis.
Adrenocortical Hyperfunction (Hyperadrenalism)
Hypercortisolism (Cushing Syndrome) is caused by any condition that produces an elevation in glucocorticoid levels. The causes of this syndrome are
A. Exogenous through administration of exogenous glucocorticoids; the most common causeB. Endogenous
1. Hypothalamic-pituitary diseases causing hypersecretion of ACTH (Cushing disease)
2. Adrenocortical hyperplasia or neoplasia
3. Ectopic ACTH secretion by nonendocrine neoplasms (paraneoplastic)
Pathological features
- The main lesions of Cushing syndrome are found in the pituitary and adrenal glands.
- The most common change in the pituitary, results from high levels of endogenous or exogenous glucocorticoids, is termed Crooke hyaline change. In this condition, the normal granular, basophilic cytoplasm of the ACTH-producing cells in the anterior pituitary is replaced by homogeneous, lightly basophilic material. This is due to accumulation of intermediate keratin filaments in the cytoplasm.
- There is one of four changes in the adrenal glands, which depends on the cause.
1. Cortical atrophy
2. Diffuse hyperplasia
3. Nodular hyperplasia
4. Adenoma, rarely a carcinoma
1. In patients in whom the syndrome results from exogenous glucocorticoids, suppression of endogenous ACTH results in bilateral cortical atrophy, due to a lack of stimulation of the cortex by ACTH. In cases of endogenous hypercortisolism, in contrast, the adrenals either are hyperplastic or contain a cortical neoplasm.
2. In Diffuse hyperplasia the adrenal cortex is diffusely thickened and yellow, as a result of an increase in the size and number of lipid-rich cells in the zonae fasciculata and reticularis.
3. Nodular hyperplasia, which takes the form of bilateral, up to 2.0-cm, yellow nodules scattered throughout the cortex.
4. Primary adrenocortical neoplasms causing Cushing syndrome may be benign or malignant. The adrenocortical adenomas are yellow tumors surrounded by capsules, and most weigh < 30 gm .
Glycogen storage diseases (glycogenoses)
1. Genetic transmission: autosomal recessive.
2. This group of diseases is characterized by a deficiency of a particular enzyme involved in either glycogen production or degradative pathways.
Diseases include:
on Gierke disease (type I)
(a) Deficient enzyme: glucose-6-phosphatase.
(b) Major organ affected by the buildup of glycogen: liver.
Pompe disease (type II)
(1) Deficient enzyme: α-glucosidase(acid maltase).
(2) Major organ affected by the buildup of glycogen: heart.
Cori disease (type III)
(1) Deficient enzyme: debranching enzyme (amylo-1,6-glucosidase).
(2) Organs affected by the buildup of glycogen: varies between the heart, liver, or skeletal muscle.
Brancher glycogenosis (type IV)
(1) Deficient enzyme: branching enzyme.
(2) Organs affected by the buildup of glycogen: liver, heart, skeletal muscle, and brain.
McArdle syndrome (type V)
(1) Deficient enzyme: muscle phosphorylase.
(2) Major organ affected by the buildup of glycogen: skeletal muscle.